title: Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells.
abstract: B cell-specific moloney murine leukemia virus integration site 1 (BMI1) is a transcriptional repressor of polycomb repressive complex 1, which is involved in the proliferation, senescence, migration, and tumorigenesis of cancer. Experimental researchers have convincingly linked BMI1 to tumorigenesis. However, there is no study about the issue on the role of BMI1 in the proliferation, apoptosis, and migration of bladder cancer. To address this question, we examined the expression of BMI1 in bladder cancer tissues and used siRNA to knockdown BMI1 expression in bladder cancer T24 cells. Then we tested the cell proliferation by CCK8 assay and soft agar colony formation assay, apoptosis by flow cytometry assay, and cell invasiveness by transwell migration assay. Our results revealed that BMI1 promoted proliferation, migration, invasion, and progression in bladder cancer. Over-expression of BMI1 was correlated with tumor clinic-pathological features. BMI1 siRNA effectively inhibited bladder cancer cell proliferation and migration in vitro, and it promoted bladder cancer invasion, maybe by causing epithelial-to-mesenchymal transition. Our findings suggested that BMI1 may represent a novel diagnostic marker and a therapeutic target for bladder cancer, and deserves further investigation.
authors.affiliation: Department of Urology, The Second Affiliated Hospital of Sun Yat-sen University, No. 107 Yan-jiang West Road, Guangzhou, Guangdong Province, 510120, People's Republic of China, doctorliangwu@sina.com.
authors.forename: Wu
authors.initials: W
authors.lastname: Liang
authors.forename: Dingjun
authors.initials: D
authors.lastname: Zhu
authors.forename: Xuejiang
authors.initials: X
authors.lastname: Cui
authors.forename: Jiarui
authors.initials: J
authors.lastname: Su
authors.forename: Hongwei
authors.initials: H
authors.lastname: Liu
authors.forename: Jinli
authors.initials: J
authors.lastname: Han
authors.forename: Fengjin
authors.initials: F
authors.lastname: Zhao
authors.forename: Wenlian
authors.initials: W
authors.lastname: Xie
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000235:genetics; D014408:Biomarkers, Tumor / Q000378:metabolism; D015820:Cadherins / Q000378:metabolism; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation; D048430:Cell Shape; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D063150:Polycomb Repressive Complex 1 / Q000378:metabolism*; D014410:Tumor Stem Cell Assay; D025803:Tumor Suppressor Protein p14ARF / Q000378:metabolism; D051879:Twist-Related Protein 1 / Q000378:metabolism; D001743:Urinary Bladder / Q000378:metabolism / Q000473:pathology; D001749:Urinary Bladder Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D014746:Vimentin / Q000378:metabolism
chemical_list: C069077:BMI1 protein, human; D014408:Biomarkers, Tumor; D015820:Cadherins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D025803:Tumor Suppressor Protein p14ARF; D051879:Twist-Related Protein 1; D014746:Vimentin; D063150:Polycomb Repressive Complex 1